Atopaxar

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种有效的、可逆的 PAR-1 拮抗剂，IC50 为 19 nM；对凝血酶和 TRAP 诱导的人血小板聚集具有有效的抑制作用，IC50 分别为 64 nM 和 31 nM。

A potent, reversible PAR-1 antagonist with IC50 of 19 nM; shows potent inhibitory effects on human platelet aggregation induced by thrombin and TRAP with IC50 of 64 nM and 31 nM, respectively, with no effect on platelet aggregation induced by either ADP or collagen; inhibits arterial thrombosis without affecting bleeding time in photochemically-induced thrombosis model guinea pigs.Thrombosis Phase 2 Clinical(In Vitro):Atopaxar (0.0001-10 μM; 1h) inhibits haTRAP (high-affinity thrombin receptor activating peptide) binding to PAR-1 on human platelet membranes in a concentration-dependent manner, with an IC50 of 0.019 μM.Atopaxar inhibits human platelet aggregation induced by thrombin or TRAP in a concentration-dependent manner.Atopaxar does not inhibit PRP (platelet-rich plasma) aggregation induced by ADP, U46619, collagen, and PAR-4ap, up to a concentration of 20 μM.(In Vivo):Atopaxar (30-100 mg/kg; p.o.) causes a dose-dependent prolongation of the time to occlusion of the femoral artery in photochemically-induced thrombosis (PIT) guinea pigs model.Atopaxar does not prolong bleeding time in guinea pigs at the highest tested dosage of 1000 mg/kg.

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Animal Model:Guinea pigs, PIT model Dosage:Oral administration Administration:10 mg/kg, 30 mg/kg, 100 mg/kg Result:Prolonged the time to occlusion by 1.8-fold and 2.4-fold at 30 mg/kg and 100 mg/kg, respectively, compared with controls.

E-5555 | E5555

GPCR/G Protein

PAR

PAR-1

Cardiovascular Disease

Thrombosis

751475-53-3

527.6374

C29H38FN3O5

>98% (HPLC)

In Vitro:?DMSO : 50 mg/mL (94.76 mM)

COC1=C(N2CCOCC2)C=C(C(CN(CC3=C4C(F)=C(OCC)C(OCC)=C3)C4=N)=O)C=C1C(C)(C)C

2-(5,6-Diethoxy-7-fluoro-1,3-dihydro-1-imino-2H-isoindol-2-yl)-1-[3-(1,1-dimethylethyl)-4-methoxy-5-(4-morpholinyl)phenyl]ethanone

(-20℃)

With Ice Pack

≥ 2 years